An energy-sparing effect of hypothermia has been described, such that
lowering the temperature may lead to increases in cardiac work
without increases in energy cost. We have recently reported improved
myocardial function with hypothermia following resuscitation from
cardiac arrest. In the present investigation, we
hypothesized that reductions in reperfusion temperature from
37°C
to
30°C
after 10 minutes of ischemia would minimize the decreases in myocyte
contractility and intracellular Ca2+ transients. Results:
Hypothermic
reperfusion following ischemia improved myocyte
contractility. Increased
myocyte intracellular
Ca2+ dynamics during hypothermia accounted for the
greater cell contractility.

We have
previously reported that hypothermia minimizes the impairment of
myocyte contractility following ischemia. In the
present study, we
investigated the mechanisms accounting for these reduced impairments
in contractility. We hypothesized that hypothermia would increase
myocyte sensitivity
to extracellular Ca2+ under
conditions of normal perfusion and following reperfusion after
ischemia.

Transthoracic impedance (TI) for defibrillation
varies widely in patients with a median value of approximately
95-100 ohms. High impedance patients are more difficult to
defibrillate. The modern generation of external defibrillators
therefore adjusts defibrillation output based on patient impedance
measurement prior to shock delivery (impedance compensation).
Commercial external defibrillators use different impedance
compensation methods (ICM). Defibrillator A (DefA, rectilinear
biphasic waveform) controls current with maximum E=200 Joules;
Defibrillator B (DefB, truncated exponential waveform) increases
shock duration with maximum E=360 Joules. The purpose of the study is to assess the effect of two
ICM on defibrillation success for TI>100ohms.Results: For TI greater than average, the current-based
compensation technique was much more efficient than the
duration-based technique; higher defibrillation current, not higher
energy from extending shock duration resulted in higher
defibrillation success.

We have previously demonstrated that
nasopharyngeal cooling (NPC) initiated during CPR improves the
success of resuscitation. In the present study, we compared the
effects of NPC with cold saline infusion (CSI) on hemodynamics,
amplitude spectrum area (AMSA) during CPR and ultimate resuscitation
outcome in a porcine model of prolonged cardiac arrest. We
hypothesized that NPC would yield better resuscitation outcome when
compared to CSI when both were initiated during CPR.

Results: In
this model, NPC improved hemodynamics and AMSA during CPR and this
was associated with increases in the success of resuscitation.

Resuscitation Blanket during CPR for
“Hands-on” Defibrillation

Uninterrupted
chest compression has been recognized as a important factor for
improving cardiopulmonary resuscitation (CPR) outcomes. We therefore
introduced a resuscitation
blanket made from insulating
material
whichallows
for uninterrupted chest compressions during shock delivery.
We hypothesized that the resuscitation blanketused
during CPR is safe, feasible and efficient to
protect the rescuer from the risk of receiving current during
defibrillation and therefore allowing performance
of
continuous chest compressions during CPR.

Results: The resuscitation blanket allows for continuous
precordial compression without interruption for delivering a
defibrillation shock. It therefore minimizes the hands-off
interruptions of chest compression and improves hemodynamics prior
to delivering of an electrical shock and ultimately increases the
defibrillation success.

Epinephrine
is administered during cardiac arrest to increase coronary perfusion
and therefore favor return
of spontaneous circulation (ROSC).Experimentally,
the a1
and b
adrenergic actions of epinephrine increase the severity of post
resuscitation myocardial dysfunction and thereby reduce the duration
of post resuscitation survival. We have previously demonstrated that
therapeutic hypothermia after
ROSC improves both post resuscitation myocardial and
neurological function. In the present study, we investigated the
combined effects of epinephrine and hypothermia. We hypothesized
that hypothermia minimizes the detrimental effects of epinephrine
on post resuscitation myocardial dysfunction and favors
survival. Results: Except for one control animal, all were
resuscitated. Post resuscitation (PR) ejection fraction (EF), neurological
deficit scores (NDS) and survivals were significantly greater after
both epinephrine and hypothermia. These findings provide
evidence that mild hypothermia minimized the adverse effects of
epinephrine on post-resuscitation neurological and myocardial
functions and favored better survival.

Comparison
between Invasive and Noninvasive Assessment of Myocardial Function
in A Rat Model of Cardiac Arrest and CPR

Placement
a pressure catheter into the left ventricle for monitoring
myocardial function is a standard technique in animal models of
cardiac arrest and CPR. However, this technique is invasive and
time-limited. We therefore sought to compare this approach with the
noninvasive echocardiographic assessment for monitoring myocardial
function in rat model of cardiac arrest and CPR. We hypothesized
that echocardiographically assessed myocardial function would be
correlated to the invasive left ventricular function measurements.

Results:All
animals were successfully resuscitated. Both dP/dt40
and EF were significantly decreased after
resuscitation (P
< 0.05). The noninvasive
assessed EF was highly correlated to dP/dt40 (R=0.75, P<0.01).The echocardiographically assessed myocardial function
is significantly correlated with the standard invasive monitoring
measurements in a rat model of cardiac arrest and CPR.

AMSA
is decreased during cardiac arrest and CPR,
in rats with chronic ischemic heart

Ventricular
fibrillation (VF) waveform features are altered in instance of acute
myocardial ischemia and chronic coronary heart disease. Amplitude
Spectrum Area (AMSA), in particular, have been investigated under
conditions of electrical induced cardiac arrest or under condition
of acute myocardial ischemia. However, no data on AMSA values during
cardiac arrest in heart suffering of chronic ischemia have been
previously investigated.In
the present study we sought to investigate AMSA during VF induced in
rats with chronic myocardial ischemia in comparison to that observed
in rats with normal myocardium. Results:AMSA
values are significantly decreased in rats with chronic ischemic
heart in comparison to those assessed in rat with not ischemic
heart.

Apoptosis
is not involved in the mechanisms of postresuscitation myocardial
dysfunction in a rat model of cardiac arrest and CPR

Postresuscitation
myocardial dysfunction (PRMD) has been recognized as the main cause
of early death after successful resuscitation from cardiac arrest.
However, the mechanisms of PRMD remain controversial. Since myocyte
apoptosisplays
an important role in myocardial dysfunction following
ischemia/reperfusion, it has also been proposed as a potential
mechanism of PRMD. We therefore investigated the presence of
apoptosis during either cardiac arrest/cardiopulmonary resuscitation
(CPR) or myocardial ischemia/reperfusion and related it to the
severity of postresuscitation myocardial dysfunction.Results: Myocardial
function was significantly impaired afterboth resuscitation
from cardiac arrest and reperfusion from LAD occlusion (P<0.01).
There was no difference in percentage of apoptotic cells between CPR
animals and sham operated animals. However, greater apoptosis
(P<0.05) was observed in animals subjected to LAD occlusion. Apoptosis,
therefore, was not involved in the mechanism of postresuscitation
myocardial dysfunction.both resuscitation
from cardiac arrest and reperfusion from LAD occlusion (P<0.01).
There was no difference in percentage of apoptotic cells between CPR
animals and sham operated animals. However, greater apoptosis
(P<0.05) was observed in animals subjected to LAD occlusion. Apoptosis,
therefore, was not involved in the mechanism of postresuscitation
myocardial dysfunction.

Both
global myocardial ischemia following cardiac arrest (CA) and
regional myocardial ischemia induced by left anterior descending
coronary artery (LAD) occlusion lead to myocardial dysfunction
following reperfusion. We therefore sought to compare myocardial
function during the reperfusion interval following resuscitation
from cardiac arrest or reperfusion from LAD occlusion. We
hypothesized that myocardial dysfunction would be more severe in
animals resuscitated from cardiac arrest in comparison to animals
subjected to LAD ligation. Results:Myocardial
dysfunction was significantly more severe following global
myocardial ischemia even though the duration of ischemia was
significantly short.

*,
P<0.05 vs LAD group; **, p<0.01 vs LAD group. ISC= ischemia

The
effects of waveform duration on efficacy of a
dual time constant biphasic truncated exponential defibrillation
waveform

The
effects of the first and the second phase durations of a biphasic
truncated exponential (BTE) waveform on defibrillation success were
evaluated in a guinea pig model of ventricular fibrillation (VF). We
hypothesized that the waveform duration, and especially the first
phase duration, plays the main role for defibrillation efficacy in
comparison to energy, current and voltage, when a dual time constant
BTE shock is employed. Results:For
dual time constant BTE waveforms, an intermediate first phase
duration, yielded
the best defibrillation efficacy with
less energy, current, and voltage
compared to shorter or longer durations.